Since it has been demonstrated that C21 steroids like pregnenolone, a non-hormonal steroid, apparently are converted in vivo by testicular tissue to testosterone it will be essential to elucidate the details of this interaction. Previous studies have indicated that once posthypophysectomy testicular atrophy occurs the tissue is unable to convert in vitro pregnenolone to testosterone. The studies described in this report indicate that pregnenolone administered in vivo at a time of hypophysectomy is converted to testosterone. We are planning to determine whether this also occurs in vitro and test the hypothesis that steroidogenic enzymes essential for conversion of pregnenolone to testosterone normally induced by gonadotropins can be maintained in absence of gonadotropins (in hypophysectomized animals) by the endogenous androgen levels. In other words, the product of pregnenolone metabolism, testosterone, is able to maintain the enzymes leading to its biogenesis. The effect of estradiol on the testes and gonadotropins will be further evaluated. Firstly it will be determined whether estradiol will block the effect of exogenously administered gonadotropins on testosterone synthesis; secondly it will be determined whether estradiol effects FSH production and release the same way it effects LH. Since it has been documented that 5 alpha-reduced androgens are capable of maintaining spermatogenesis in hypophysectomized animals and inducing the initiation of the spermatogenic process in immature animals the details of these relationships will be evaluated and the role of FSH in this process will be determined.